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Special Issue "Physiological or Pathological Molecular Alterations in Brain Aging"

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 22595

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Special Issue Editors

Dr. Marika Cordaro

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Guest Editor

Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, 98125 Messina, Italy
Interests: physiology; metabolites; inflammation; pathology; neurology
Special Issues, Collections and Topics in MDPI journals

Dr. Rossana Morabito

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Co-Guest Editor

Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, 98166 Messina, Italy
Interests: physiology; ion trasport; band 3 protein; erythrocytes; oxidative stress; aging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Aging is defined as a progressive time‐related accumulation of changes involved in the increased susceptibility to disease and death. The brain seems to be particularly sensitive to the aging process since the appearance of neurodegenerative diseases, including Alzheimer's disease, Parkinson’s Disease, Vascular Dementia and many others, are exponential with the increasing age. There has been extensive research into these common diseases with a focus on establishing the etiology and developing therapies for their treatment and, most important, their prevention.

This Special Issue on “Physiological or pathological molecular alteration in brain aging” aims to cover all aspects of brain studies and health promotion and prevention, such as studies on mitochondrial dysfunction, autophagy, oxidative stress and inflammation associated with brain disorders.

In addition, we also welcome studies on pharmacological or phytochemical or nutraceutical effects of compounds that are able to counteract the impact of the age in the brain.

Research articles collecting data from both in vitro and in vivo investigations are appreciated, as are full reviews, including news in the field of the current understanding of molecular mechanisms involved in the brain during aging.

Dr. Marika Cordaro
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

brain
aging
oxidative stress
autophagy
mitochondrial dysfunction
neurological disorders
neurodegeneration
neuroinflammation

Published Papers (7 papers)

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Editorial

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Open AccessEditorial

Physiological or Pathological Molecular Alterations in Brain Aging

Rossana Morabito

and

Marika Cordaro

Int. J. Mol. Sci. 2022, 23(15), 8601; https://doi.org/10.3390/ijms23158601 - 02 Aug 2022

Viewed by 1078

Abstract

Aging is a natural phenomenon that occurs due to a variety of loosely understood mechanisms [...] Full article

(This article belongs to the Special Issue Physiological or Pathological Molecular Alterations in Brain Aging)

Research

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Open AccessArticle

Epigenetic Studies in the Male APP/BIN1/COPS5 Triple-Transgenic Mouse Model of Alzheimer’s Disease

Olaia Martínez-Iglesias

Vinogran Naidoo

Iván Carrera

and

Ramón Cacabelos

Int. J. Mol. Sci. 2022, 23(5), 2446; https://doi.org/10.3390/ijms23052446 - 23 Feb 2022

Cited by 4 | Viewed by 1723

Abstract

Alzheimer’s Disease (AD) is a major health problem worldwide. The lack of efficacy of existing therapies for AD is because of diagnosis at late stages of the disease, limited knowledge of biomarkers, and molecular mechanisms of AD pathology, as well as conventional drugs that are focused on symptomatic rather than mechanistic features of the disease. The connection between epigenetics and AD, however, may be useful for the development of novel therapeutics or diagnostic biomarkers for AD. The aim of this study was to investigate a pathogenic role for epigenetics and other biomarkers in the male APP/BIN1/COPS5 triple-transgenic (3xTg) mouse model of AD. In the APP/BIN1/COPS5 3xTg-AD mouse hippocampus, sirtuin expression and activity decreased, HDAC3 expression and activity increased, PSEN1 mRNA levels were unchanged, PSEN2 and APOE expression was reduced, and levels of the pro-inflammatory marker IL-6 increased; levels of pro-inflammatory COX-2 and TNFα and apoptotic (NOS3) markers increased slightly, but these were non-significant. In fixed mouse-brain slices, immunoreactivity for CD11b and β-amyloid immunostaining increased. APP/BIN1/COPS5 3xTg-AD mice are a suitable model for evaluating epigenetic changes in AD, the discovery of new epigenetic-related biomarkers for AD diagnosis, and new epidrugs for the treatment of this neurodegenerative disease. Full article

(This article belongs to the Special Issue Physiological or Pathological Molecular Alterations in Brain Aging)

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Open AccessArticle

Atrazine Inhalation Causes Neuroinflammation, Apoptosis and Accelerating Brain Aging

Alessio Filippo Peritore

Angela Trovato Salinaro

Marika Cordaro

and

Rosanna Di Paola

Int. J. Mol. Sci. 2021, 22(15), 7938; https://doi.org/10.3390/ijms22157938 - 26 Jul 2021

Cited by 15 | Viewed by 2373

Abstract

Background: exposure to environmental contaminants has been linked to an increased risk of neurological diseases and poor outcomes. Chemical name of Atrazine (ATR) is 6-chloro-N-ethyl-N′-(1-methylethyl)-1,3,5-triazine-2,4-diamine, and it is the most commonly used broad-spectrum herbicide in agricultural crops. Several studies have demonstrated that ATR has the potential to be harmful to the brain’s neuronal circuits. Until today nobody has explored the effect of ATR inhalation on young and aged mice. Methods: young and aged mice were subject to 25 mg of ATR in a vehicle made with saline and 10% of Dimethyl sulfoxide (DMSO) every day for 28 days. At the end of experiment different behavioral test were made and brain was collected. Results: exposure to ATR induced the same response in terms of behavioral alterations and motor and memory impairment in mice but in aged group was more marked. Additionally, in both young and aged mice ATR inhalations induced oxidative stress with impairment in physiological antioxidant response, lipid peroxidation, nuclear factor kappa-light-chain-enhancer of activated B cells (nf-κb) pathways activation with consequences of pro-inflammatory cytokines release and apoptosis. However, the older group was shown to be more sensitive to ATR inhalation. Conclusions: our results showed that aged mice were more susceptible compared to young mice to air pollutants exposure, put in place a minor physiologically response was seen when exposed to it. Full article

(This article belongs to the Special Issue Physiological or Pathological Molecular Alterations in Brain Aging)

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Open AccessArticle

Selective Activation of CNS and Reference PPARGC1A Promoters Is Associated with Distinct Gene Programs Relevant for Neurodegenerative Diseases

Emanuele Bernardinelli

and

Int. J. Mol. Sci. 2021, 22(7), 3296; https://doi.org/10.3390/ijms22073296 - 24 Mar 2021

Cited by 6 | Viewed by 2798

Abstract

The transcriptional regulator peroxisome proliferator activated receptor gamma coactivator 1A (PGC-1α), encoded by PPARGC1A, has been linked to neurodegenerative diseases. Recently discovered CNS-specific PPARGC1A transcripts are initiated far upstream of the reference promoter, spliced to exon 2 of the reference gene, and are more abundant than reference gene transcripts in post-mortem human brain samples. The proteins translated from the CNS and reference transcripts differ only at their N-terminal regions. To dissect functional differences between CNS-specific isoforms and reference proteins, we used clustered regularly interspaced short palindromic repeats transcriptional activation (CRISPRa) for selective endogenous activation of the CNS or the reference promoters in SH-SY5Y cells. Expression and/or exon usage of the targets was ascertained by RNA sequencing. Compared to controls, more differentially expressed genes were observed after activation of the CNS than the reference gene promoter, while the magnitude of alternative exon usage was comparable between activation of the two promoters. Promoter-selective associations were observed with canonical signaling pathways, mitochondrial and nervous system functions and neurological diseases. The distinct N-terminal as well as the shared downstream regions of PGC-1α isoforms affect the exon usage of numerous genes. Furthermore, associations of risk genes of amyotrophic lateral sclerosis and Parkinson’s disease were noted with differentially expressed genes resulting from the activation of the CNS and reference gene promoter, respectively. Thus, CNS-specific isoforms markedly amplify the biological functions of PPARGC1A and CNS-specific isoforms and reference proteins have common, complementary and selective functions relevant for neurodegenerative diseases. Full article

(This article belongs to the Special Issue Physiological or Pathological Molecular Alterations in Brain Aging)

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Review

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Open AccessReview

Health Benefits Related to Tree Nut Consumption and Their Bioactive Compounds

and

Int. J. Mol. Sci. 2021, 22(11), 5960; https://doi.org/10.3390/ijms22115960 - 31 May 2021

Cited by 29 | Viewed by 4382

Abstract

Long-term studies with regular tree nut consumption have indicated positive outcomes for multiple health benefits. Here, we review the beneficial effects of tree nuts, highlighting the impact on glucose modulation, body weight management, cardiovascular risk, inflammation, oxidative stress, cognitive performance, and gut microbiota. Nuts are important sources of nutrients and phytochemicals, which, together with a healthy lipid profile, could help prevent certain chronic diseases, protect against oxidative stress and inflammation, and improve cognitive performance, thus reducing the impact of aging and neurodegeneration. Full article

(This article belongs to the Special Issue Physiological or Pathological Molecular Alterations in Brain Aging)

Open AccessReview

Senescent Microglia: The Key to the Ageing Brain?

Eleanor K. Greenwood

and

David R. Brown

Int. J. Mol. Sci. 2021, 22(9), 4402; https://doi.org/10.3390/ijms22094402 - 22 Apr 2021

Cited by 21 | Viewed by 5218

Abstract

Ageing represents the single biggest risk factor for development of neurodegenerative disease. Despite being such long-lived cells, microglia have been relatively understudied for their role in the ageing process. Reliably identifying aged microglia has proven challenging, not least due to the diversity of cell populations, and the limitations of available models, further complicated by differences between human and rodent cells. Consequently, the literature contains multiple descriptions and categorisations of microglia with neurotoxic phenotypes, including senescence, without any unifying markers. The role of microglia in brain homeostasis, particularly iron storage and metabolism, may provide a key to reliable identification. Full article

(This article belongs to the Special Issue Physiological or Pathological Molecular Alterations in Brain Aging)

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Open AccessReview

Mitophagy and the Brain

Natalie S. Swerdlow

and

Heather M. Wilkins

Int. J. Mol. Sci. 2020, 21(24), 9661; https://doi.org/10.3390/ijms21249661 - 18 Dec 2020

Cited by 28 | Viewed by 4065

Abstract

Stress mechanisms have long been associated with neuronal loss and neurodegenerative diseases. The origin of cell stress and neuronal loss likely stems from multiple pathways. These include (but are not limited to) bioenergetic failure, neuroinflammation, and loss of proteostasis. Cells have adapted compensatory mechanisms to overcome stress and circumvent death. One mechanism is mitophagy. Mitophagy is a form of macroautophagy, were mitochondria and their contents are ubiquitinated, engulfed, and removed through lysosome degradation. Recent studies have implicated mitophagy dysregulation in several neurodegenerative diseases and clinical trials are underway which target mitophagy pathways. Here we review mitophagy pathways, the role of mitophagy in neurodegeneration, potential therapeutics, and the need for further study. Full article

(This article belongs to the Special Issue Physiological or Pathological Molecular Alterations in Brain Aging)

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